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Samara L Lewis

Publications and source records attributed to Samara L Lewis.

5 recordsLinked to original sources
PubMed2006

Sequential allocation and global pattern of movement of the definitive endoderm in the mouse embryo during gastrulation.

During mouse gastrulation, endoderm cells of the dorsal foregut are recruited ahead of the ventral foregut and move to the anterior region of the embryo via different routes. Precursors of the anterior-most part of the foregut and those of the mid- and hind-gut are allocated to the endoderm of the mid-streak-stage embryo, whereas the precursors of the rest of the foregut are recruited at later stages of gastrulation. Loss of Mixl1 function results in reduced recruitment of the definitive endoderm, and causes cells in the endoderm to remain stationary during gastrulation. The observation that the endoderm cells are inherently unable to move despite the expansion of the mesoderm in the Mixl1-null mutant suggests that the movement of the endoderm and the mesoderm is driven independently of one another.

Animals↗
PubMed2006

Genetic interaction of Gsc and Dkk1 in head morphogenesis of the mouse.

Mouse embryos lacking Gsc and Dkk1 function display severe deficiencies in craniofacial structures which are not found in either Dkk1 homozygous null or Gsc homozygous null mutant embryos. Loss of Gsc has a dosage-related effect on the severity of head truncation phenotype in Dkk1 heterozygous embryos. The synergistic effect of these mutations in enhancing head truncation provides direct evidence of a genetic interaction between Gsc and Dkk1, which display overlapping expression in the prechordal mesoderm. In the absence of Gsc activity, the expression of Dkk1, WNT genes and a transgenic reporter for WNT signalling are altered. Our results show that Gsc and Dkk1 functions are non-redundant in the anterior mesendoderm for normal anterior development and Gsc may influence Wnt signalling as a negative regulator.

Journal Article↗
PubMed2006

Definitive endoderm of the mouse embryo: formation, cell fates, and morphogenetic function.

The endoderm is one of the primary germ layers but, in comparison to ectoderm and mesoderm, has received less attention. The definitive endoderm forms during gastrulation and replaces the extraembryonic visceral endoderm. It participates in the complex morphogenesis of the gut tube and contributes to the associated visceral organs. This review highlights the role of the definitive endoderm as a source of patterning cues for the morphogenesis of other germ-layer tissues, such as the anterior neurectoderm and the pharyngeal region, and also emphasizes the intricate patterning that the endoderm itself undergoes enabling the acquisition of regionalized cell fates.

Animals↗
PubMed2004

Isolation and embryonic expression of avian ADAM 12 and ADAM 19.

Members of the ADAM gene family encode large multi-domain proteins containing A Disintegrin And Metalloprotease domain. We have cloned quail orthologs of ADAM 12 and 19 using PCR-based screening and describe their expression patterns over the period E2.5 (Hamilton and Hamburger stage 14) to E5.0 (HH 25) using in situ hybridisation. Quail ADAM 12 is expressed in mesenchyme, cranially, in the tail and in the limb buds, and also in visceral mesenchyme. In the nervous system it is expressed in dorsal root ganglia and ventral roots. Quail ADAM 19 is expressed in cranial and dorsal root ganglia, sympathetic ganglia, ventral mixed nerves and in the allantois. Avian ADAM 12 and 19 genes exhibit similarities and differences in expression pattern compared to their murine orthologs, for example, expression of ADAM 12 in the nervous system, limb and tail bud in quail but not mouse. Interestingly, in mouse ADAM 19 is expressed in these locations. We have generated a sheep antibody to quail ADAM 19 and, in embryonic cells in vitro, found the protein at cell-cell junctions in many cell types. Some of these did have detectable ADAM 19 by in situ hybridisation but RT-PCR analysis confirmed the presence of low level ADAM 19 transcripts not detectable by in situ hybridisation.

ADAM Proteins↗